ArticleCirculation. Arrhythmia and electrophysiology2014
Caveolin-1 modulates cardiac gap junction homeostasis and arrhythmogenecity by regulating cSrc tyrosine kinase.
Article in Circulation. Arrhythmia and electrophysiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 41 citations in OpenAlex.
- Preoperative Activation of c-Src Kinase in Atrial Tissue in Patients Developing Postoperative Atrial Fibrillation.Medicina (Kaunas, Lithuania) · 2025Article
- S-Nitrosylation in Cardiovascular Disorders: The State of the Art.Biomolecules · 2025Review
- Protective Effects of Low-Intensity Pulsed Ultrasound on Cardiac Electrophysiological Function in a Rat Model of Ischemic Cardiomyopathy.Journal of the American Heart Association · 2025Article
- c-Src Is Responsible for Mitochondria-Mediated Arrhythmic Risk in Ischemic Cardiomyopathy.Circulation. Arrhythmia and electrophysiology · 2024Article
- Interplay between caveolin-1 and mineralocorticoid receptor in cardiometabolic disease.The Journal of endocrinology · 2024Review
- Global chromatin landscapes identify candidate noncoding modifiers of cardiac rhythm.The Journal of clinical investigation · 2023Article
- Caveolin-3 and Arrhythmias: Insights into the Molecular Mechanisms.Journal of clinical medicine · 2022Review
- Exploration of Mechanisms of Sacubitril/Valsartan in the Treatment of Cardiac Arrhythmias Using a Network Pharmacology Approach.Frontiers in cardiovascular medicine · 2022Article
- Tunable electroconductive decellularized extracellular matrix hydrogels for engineering human cardiac microphysiological systems.Biomaterials · 2021Article
- Cardiac Connexin-43 Hemichannels and Pannexin1 Channels: Provocative Antiarrhythmic Targets.International journal of molecular sciences · 2020Review
- Potential causal association of a prolonged PR interval and clinical recurrence of atrial fibrillation after catheter ablation: a Mendelian randomization analysis.Journal of human genetics · 2020Article
- Dietary α-Linolenic Acid Counters Cardioprotective Dysfunction in Diabetic Mice: Unconventional PUFA Protection.Nutrients · 2020Article
- Role of Caveolin-1 in Diabetes and Its Complications.Oxidative medicine and cellular longevity · 2020Review
- Karoshi May Be a Consequence of Overwork-Related Malignant Arrhythmia.Medical science monitor : international medical journal of experimental and clinical research · 2019Article
- Caveolins as Regulators of Stress Adaptation.Molecular pharmacology · 2018Review
- Environmental Toxicant Exposures and Type 2 Diabetes Mellitus: Two Interrelated Public Health Problems on the Rise.Current opinion in toxicology · 2018Article
- Sarcolemmal dependence of cardiac protection and stress-resistance: roles in aged or diseased hearts.British journal of pharmacology · 2016Review
- Src-dependent phosphorylation of caveolin-1 Tyr-14 promotes swelling and release of caveolae.Molecular biology of the cell · 2016Article
- Genetic variations involved in sudden cardiac death and their associations and interactions.Heart failure reviews · 2016Review
- Regulation of gap junction channels and hemichannels by phosphorylation and redox changes: a revision.BMC cell biology · 2016Review
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
backgroundGenome-wide association studies have revealed significant association of caveolin-1 (Cav1) gene variants with increased risk of cardiac arrhythmias. Nevertheless, the mechanism for this linkage is unclear. METHODS AND
resultsUsing adult Cav1(-/-) mice, we revealed a marked reduction in the left ventricular conduction velocity in the absence of myocardial Cav1, which is accompanied with increased inducibility of ventricular arrhythmias. Further studies demonstrated that loss of Cav1 leads to the activation of cSrc tyrosine kinase, resulting in the downregulation of connexin 43 and subsequent electric abnormalities. Pharmacological inhibition of cSrc mitigates connexin 43 downregulation, slowed conduction, and arrhythmia inducibility in Cav1(-/-) animals. Using a transgenic mouse model with cardiac-specific overexpression of angiotensin-converting enzyme (ACE8/8), we demonstrated that, on enhanced cardiac renin-angiotensin system activity, Cav1 dissociated from cSrc because of increased Cav1 S-nitrosation at Cys(156), leading to cSrc activation, connexin 43 reduction, impaired gap junction function, and subsequent increase in the propensity for ventricular arrhythmias and sudden cardiac death. Renin-angiotensin system-induced Cav1 S-nitrosation was associated with increased Cav1-endothelial nitric oxide synthase binding in response to increased mitochondrial reactive oxidative species generation.
conclusionsThe present studies reveal the critical role of Cav1 in modulating cSrc activation, gap junction remodeling, and ventricular arrhythmias. These data provide a mechanistic explanation for the observed genetic link between Cav1 and cardiac arrhythmias in humans and suggest that targeted regulation of Cav1 may reduce arrhythmic risk in cardiac diseases associated with renin-angiotensin system activation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.